Mechanism of action

Clarithromycin prevents bacteria Irom growing by interIering with their protein synthesis.
Clarithromycin binds to the subunit 50S oI the bacterial ribosome and thus inhibits the
translation oI peptides. Clarithromycin has similar antimicrobial spectrum as erythromycin but is
more eIIective against certain gram-negative bacteria, particularly Legionella pneumophila.
Besides this bacteriostatic eIIect, clarithromycin also has bactericidal eIIect on certain strains
such as Haemophilus influen:ae, Streptococcus pneumoniae and Neisseria gonorrhoeae.
edit] Pharmacokinetics
&nlike erythromycin, clarithromycin is acid-stable and can thereIore be taken orally without
being protected Irom gastric acids. It is readily absorbed, and diIIused into most tissues and
phagocytes. Due to the high concentration in phagocytes, clarithromycin is actively transported
to the site oI inIection. During active phagocytosis, large concentrations oI clarithromycin are
released. The concentration oI clarithromycin in the tissues can be over 10 times higher than in
plasma. Highest concentrations were Iound in liver and lung tissue.
edit] Metabolism
Clarithromycin has a Iairly rapid Iirst-pass hepatic metabolism. However, 14-hydroxy
clarithromycin, clarithromycin's metabolite, is almost twice as active and has a halI liIe oI 7
hours compared to clarithromycin's 5. Clarithromycin and its metabolites main routes oI
elimination are urinary and biliary excretion. OI all the drugs in its class, clarithromycin has the
best bioavailability at 50, which makes it amenable to oral administration.
CeIuroxime axetil
CeIuroxime is a second generation cephalosporin with a broad antimicrobial activity against both
Gram-positive and Gram-negative organisms. It has excellent in vitro activity against
staphylococcal strains, streptococcal strains (other than enterococci), N. gonorrhoeae, H.
inIluenzae and N. meningitidis. It also has excellent in vitro activity against members oI the
Enterobacteriaceae with the exception oI Serratia and indole-positive Proteus. Ps. aeruginosa and
B. Iragilis are resistant. CeIuroxime is relatively Iree oI serious side eIIects. It is metabolically
stable, and most oI it is excreted unchanged in the urine. Three Iourths oI it are distributed in the
extravascular compartment. Blood levels exceed the in vitro minimum inhibitory concentrations
Ior many important gram negative pathogens. Clinical studies have shown ceIuroxime to be
eIIective therapy Ior inIections oI soIt tissue, respiratory tract, urinary tract, genital tract (caused
by N. gonorrhoeae) and the central nervous system. SuperinIections with Ps. aeruginosa and
enterococcal strains may present a problem. In spite oI excellent diIIusion into bone and joint
tissues, the available clinical data are too limited to make a recommendation Ior its use in bone
and joint inIections.

Bactericidal: inhibits synthesis of bacterial cell wall, causing cell death.
CeIuroxime, like the penicillins, is a beta-lactam antibiotic. By binding to speciIic penicillin-
binding proteins (PBPs) located inside the bacterial cell wall, it inhibits the third and last stage oI
bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes
such as autolysins; it is possible that ceIuroxime interIeres with an autolysin inhibitor.



D&'ENT
Ipratropium bromide- salbutamolIixed-dose combination (FDC) maximizes the response to
treatment in patients with bronchial asthma and chronic obstructive pulmonary disease (COPD)
by increasing bronchodilation through 2 distinctly diIIerent mechanisms
ie,
anticholinergic(parasympatholytic) and 2-agonist (sympathomimetic) eIIects. Simultaneous
administration oI both an anticholinergic (ipratropium bromide) and a 2- sympathomi metic
(salbutamol sulIate) produces a greater bronchodilat or eIIect than when either drug is used
alone.

Duavent increases broncho-dilation ,decreaslng reslsLance ln Lhe resplraLory alrway and lncreaslng
alrflow Lo Lhe lungs thus prevents wheezing, diIIiculty oI breathing, chest tightness and coughing.

eople wlLh asthma have Lrouble breaLhlng because Lhelr alrways are lnflamed and become narrowed
normally alr moves smooLhly from Lhe mouLh and nose Lhrough Lhe alrways and lnLo Lhe Llny alr sacs of
Lhe lungs as a person breaLhes ln 8reaLhlng ouL (exhallng) happens auLomaLlcally when Lhe person
sLops breaLhlng ln ln a person wlLh asLhma breaLhlng ln (lnhallng) ls noL a problem lncomlng alr can
sllde around Lhe blockage because Lhe acL of breaLhlng ln makes Lhe alrways expand 1he problem
comes when Lhe person wlLh asLhma Lrles Lo breaLhe ouL 1he alr can no longer geL pasL Lhe blockage
and lL remalns Lrapped ln Lhe lungs 1he person can Lhen only Lake shallow breaLhs 8ronchodllaLors
work by relaxlng Lhe smooLh muscles LhaL llne Lhe alrways 1hls makes Lhe alrways open wlder and
allows alr Lo leave Lhe lungs 1hese drugs also are used Lo relleve breaLhlng problems assoclaLed wlLh
emphysema chronlc bronch|t|s and oLher lung dlseases